Interpretive Summary: Root-Knot nematodes are major pests of solanaceous crops, including Tomato and Potato. This study identifies mechanisms involved in host-resistance to root-knot nematodes. Results suggested that jasmonate-dependent signaling does not play a role in Mi-1 mediated nematode defense, but does play a role in basal defense against root-knot nematodes. Microarray analysis identified 1497 genes differentially regulated 24 hours after root-knot infection in resistant plants and 750 genes differentially regulated in susceptible plants.

Technical Abstract:
Response of tomato (Solanum lycopersicum) to root-knot nematode (RKN; Meloidogyne spp.) infection was monitored using TOM1 cDNA microarray with resistant (‘Motelle’; Mi-1) and susceptible (‘Moneymaker’; mi) tomato at 24 h after RKN infection. The array analysis identified 1497 genes and 750 genes differentially regulated (P < 0.05) in the incompatible and compatible interactions, respectively. Thirty seven percent of the differentially regulated genes were specific to the incompatible interactions. In the incompatible interactions, 880 genes were 2-fold up-regulated and 332 were 1.5-fold down-regulated. In the compatible interactions, 677 were 2-fold up-regulated and 62 were 1.5-fold down-regulated. Both jasmonic acid (JA) biosynthetic genes and JA-regulated genes were up-regulated in both compatible and incompatible interactions. Of the limited number of known salicylic acid (SA)-regulated genes present on the array, majority was regulated in both interactions. To test a role for JA and SA signaling pathways in both Mi-1 resistance and basal defense to RKN, the jai1 mutant and NahG transgenic line were used in the presence or absence of the RKN resistance gene Mi-1. RKN did not reproduce on Mi-1 jai1 plants and reproduced less on jai1 mutant compared to the wild-type parent ‘CM’. Similarly, RKN did not reproduce on Mi-1 NahG plants and reproduced at similar levels on NahG and wild-type parent ‘Moneymaker’. No detectable increases in SA levels were detected after RKN infection of jai1 roots. Our results suggest that JA-dependent signaling does not play a role in Mi-1-mediated defense but plays a role in basal defense against RKN in tomato.